Subcellular distribution of phospholipids during liver damage induced by rare earths

Lehmann, B.; Oberdisse, E; Grajewski, O.; Arntz, Hans-Richard

doi:10.1007/bf00353309

Cited by 14 publications

(3 citation statements)

References 29 publications

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“…It is well known that phospholipid is an important component of very low density lipoproteins. And the changes of blood lipoprotein caused by Ln 3+ were due to the inhibition of apoprotein synthesis [31]. Previous researches demonstrated that the liver which is subjected to fatty degeneration caused by Ln 3+ could not oxidize octanoic acid [30] and was thought that Ln 3+ interfered with the synthesis of ATP and the activation of fatty acid in the liver [32].…”

Section: Discussionmentioning

confidence: 99%

Organ Histopathological Changes and its Function Damage in Mice Following Long-term Exposure to Lanthanides Chloride

Cheng

Cai

et al. 2011

Biol Trace Elem Res

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Due to increasing applications of lanthanides (Ln) in industry and daily life, numerous studies confirmed that Ln exposure may result in organ damages in mice and rats, while very few studies focused on several organs damages simultaneously. In order to compare the toxicity of Ln on organs, mice were exposed to LaCl(3), CeCl(3), and NdCl(3) of a dose of 20 mg/kg body weight for consecutive 60 days, respectively, then histopathological changes of liver, kidney, and heart, and their function were investigated. The results showed that long-term exposure to Ln caused cell necrosis and basophilia of liver, ambiguity of renal tubule architecture, congestion of blood vessel and capillary of kidney, and heart hemorrhage. The histopathological changes of liver, kidney, and heart in mice caused by Ce(3+) was most severe; the effect by Nd(3+) was slighter than Ce(3+) but more severe than La(3+). The assay of serum biochemical parameters suggested that Ln exposure severely impaired the functions of liver, kidney, and myocardium in mice. These findings suggested that long-term exposure to Ln resulted in histopathological changes of liver, kidney, and heart, and their function damages. Therefore, we thought that long-term application of the products containing Ln on human should be cautious.

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Section: Discussionmentioning

confidence: 99%

Organ Histopathological Changes and its Function Damage in Mice Following Long-term Exposure to Lanthanides Chloride

Cheng

Cai

et al. 2011

Biol Trace Elem Res

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show abstract

“…It is well known that phospholipid is an important component of very low-density lipoproteins. The changes of blood lipoprotein caused by Ln 3+ were due to the inhibition of apoprotein synthesis [37]. Previous researches demonstrated that the liver subjected to fatty degeneration caused by Ln 3+ could not oxidize octanoic acid [38], and suggested that Ln 3+ interfered with the synthesis of ATP and the activation of fatty acid in the liver [39].…”

Section: Discussionmentioning

confidence: 99%

“…The main toxicological and biochemical effects caused by light rare earths were attributed to the generation of fatty liver, and the fatty infiltration caused by light rare earths was due to rapid mobilization of stored lipid [12]. Pr 3+ could cause blood lipid metabolism disorders in mice [36] and reduce phospholipid secretion in liver [37]. It is well known that phospholipid is an important component of very low-density lipoproteins.…”

Section: Discussionmentioning

confidence: 99%

The Mechanism of Liver Injury in Mice Caused by Lanthanoids

Fei

et al. 2010

Biol Trace Elem Res

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It has been proven that higher dose of lanthanoid (Ln) can induce liver toxicities, but the mechanisms and the molecular pathogenesis are still unclear. In this study, LaCl₃, CeCl₃, and NdCl₃ at a higher dose of 20 mg/kg body weight was injected into the abdominal cavity of ICR mice for 14 consecutive days, and the inflammatory responses of liver of mice were investigated by histopathological test, real-time quantitative reverse transcription polymerase chain reaction (RT-PCR), and enzyme-linked immunosorbent assay (ELISA) methods. The results showed the significant accumulation of Ln in the liver results in liver histopathological changes and, therefore, liver malfunctions. The real-time quantitative RT-PCR and ELISA analyses showed that Ln could significantly alter the mRNA and protein expressions of several inflammatory cytokines, including nucleic factor-κB, macrophage migration inhibitory factor, tumor necrosis factor-α, interleukin-1β, interleukin-6, cross-reaction protein, interleukin-4, and interleukin-10. Our results also implied that the inflammatory responses and liver injury likely are caused by 4f shell and alterable valence properties of Ln-induced liver toxicity.

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Metal ion release from paramagnetic chelates: What is tolerable?

Rocklage¹,

Worah²,

Kim³

1991

Magnetic Resonance in Med

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At the currently administered clinical doses, paramagnetic metal chelate complexes presently used as MR contrast enhancement agents appear to be relatively nontoxic. Solution thermodynamic, solubility, and selectivity studies, based on a number of gadolinium chelate complexes, indicate that very little gadolinium is released in vivo, and the small amounts that do remain are available for excretion, albeit slowly. Although the mechanism of metal release from manganese-based chelate complexes is not well understood, any released manganese is likely to be quickly and efficiently cleared through the liver. Although MRI contrast agents are unlikely to be administered repeatedly in patients, which could result in accumulation of metal ion, the long-term effects of such potential deposition have yet to be demonstrated.

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Subcellular distribution of phospholipids during liver damage induced by rare earths

Cited by 14 publications

References 29 publications

Organ Histopathological Changes and its Function Damage in Mice Following Long-term Exposure to Lanthanides Chloride

Organ Histopathological Changes and its Function Damage in Mice Following Long-term Exposure to Lanthanides Chloride

The Mechanism of Liver Injury in Mice Caused by Lanthanoids

Metal ion release from paramagnetic chelates: What is tolerable?

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